Causal and common risk pathways linking childhood maltreatment to later intimate partner violence victimization

Childhood maltreatment and intimate partner violence (IPV) victimization are major psychiatric risk factors. Maltreatment substantially increases the likelihood of subsequent IPV victimization, but what drives this association is poorly understood. We analyzed retrospective self-reports of maltreatment and IPV in 12794 participants (58% women, 42% men) from the Twins Early Development Study at ages 21 and 26 using quantitative genetic methods. We estimated the etiological influences common to maltreatment and IPV, and the direct causal effect of maltreatment on IPV beyond such common influences. Participants exposed to maltreatment (~7% of the sample) were 3 times more likely to experience IPV victimization than their peers at age 21, 4 times more likely at 26. The association between maltreatment and IPV was mostly due to environmental influences shared by co-twins (42-43%) and genetic influences (30–33%). The association between maltreatment and IPV was similar for women and men, but its etiology partly differed by sex. Maltreatment had a moderate-to-large effect on IPV in phenotypic models (β = 0.23–0.34), decreasing to a small-to-moderate range in causal models accounting for their common etiology (β = 0.15–0.21). Risk factors common to maltreatment and IPV victimization are largely familial in origin, environmental and genetic. Even considering common risk factors, experiencing maltreatment is causally related to subsequent IPV victimization. Interventions promoting safe intimate relationships among young adults exposed to maltreatment are warranted and should address family-level environmental risk and individual-level risk shaped by genetics.


Introduction
Globally, about 20% of adults report experiencing at least one form of maltreatment by parents or caregivers before age 16, with prevalence rates varying across types of maltreatment, such as abuse and neglect (1-4).Childhood maltreatment (hereafter, maltreatment) is a major risk factor for psychiatric disorders, substantially adding to the global burden of disease (5,6).Furthermore, individuals exposed to maltreatment face a higher risk of experiencing interpersonal violence later in life compared to their peersa phenomenon known as "revictimization" (7)(8)(9)(10)(11).
A critical form of revictimization after maltreatment is intimate partner violence (IPV), with individuals exposed to maltreatment being 3-6 times more likely to experience IPV from age 16 than their peers (12,13).It has been estimated that about 20-30% of adults experience some form of IPV victimization throughout their lives (14,15), but this prevalence can rise up to 77% among those exposed to maltreatment (16).IPV occurs in heterosexual and homosexual relationships to a similar extent (17)(18)(19).Some studies report higher prevalence rates of IPV victimization in women than men, particularly more sexual abuse (20)(21)(22), while others report comparable estimates, particularly for physical abuse (23,24).What is noteworthy is that individuals exposed to maltreatment face heightened risk of IPV victimization and that this is true for different sexual orientations and sexes (12,(25)(26)(27).Akin to maltreatment, IPV victimization increases psychiatric risk (28,29).Moreover, experiencing both maltreatment and IPV has a more detrimental impact on mental health than either experience alone (30,31).In light of this evidence base, elucidating the underlying processes linking maltreatment to IPV is critical to develop effective preventative interventions.

Possible pathways from childhood maltreatment to intimate partner violence victimization
The prevailing hypothesis regarding the association between maltreatment and IPV proposes that maltreatment initiates processes that are, in turn, causally related to IPV (Figure 1, red and blue paths).This is in line with state dependence theories of revictimization, which postulate that victimization can lead to changes in an individual that increase their risk of revictimization (32,33).
Cross-sectional population-based data hints at a number of psychological (e.g.emotional dysregulation (34,35)) and social processes (e.g., relationship quantity and quality (36,37)) that partly, but modestly, mediate the association between maltreatment and IPV.However, formal examinations of putative causal effects of maltreatment on IPV are lacking.
An alternative hypothesis postulates that the association between separate victimization eventssuch as between maltreatment and IPVis non-causal and, rather, driven by shared time-stable risk factors IPV (green path).This is consistent with the population heterogeneity theory of revictimization (32,38).Evidence that maltreatment and IPV share a number of common risk factors lends support to this hypothesis.For example, population-based studies indicate that environmental risk factors like socioeconomic disadvantage place individuals at risk of both maltreatment (39,40) and IPV (41,42).However, systematic reviews and meta-analyses indicate that psychological vulnerabilities have an even greater effect size than environmental factors on the risk of maltreatment (43,44) and IPV (45)(46)(47).Since similar environmental and psychological factors may increase risk of both maltreatment and IPV, the putative causal effect of maltreatment on IPV beyond their shared etiology should be examined.

The utility of genetically informed designs to disentangle risk pathways to revictimization
Extant research suggests that both causal pathways and common risk factors are likely to contribute to the association between maltreatment and IPV victimization.Studies using phenotypic methods like structural equation modelling and multivariable logistic regression indicate a persisting effect of maltreatment on IPV, even when accounting for specific individual-(e.g., aggressive behavior) and family-level factors (e.g., social deprivation) known to confer risk to both experiences (48)(49)(50).However, phenotypic methods may overestimate the impact of maltreatment on IPV because they can only account for a finite number of common risk factors.Genetically informed designs like the twin design provide a quasi-experimental framework to estimate the common etiology between maltreatment and IPV, and to examine their causal relationships beyond such common etiology, without measuring specific common risk factors (51,52).Studies using genetically informed designs indicate, for instance, that maltreatment has a small additional effect on mental health problems beyond its common etiology with mental health problems (53,54).
The twin design has been employed to investigate the etiology of maltreatment and IPV separately, by comparing the experiences monozygotic and dizygotic twins, who differ in their genetic resemblance.Twin studies have shown that genetic factors and environmental exposures that make co-twins dissimilar ("nonshared" environment) each explain a moderate-to-large proportion of individual differences in maltreatment (40-60%), with environmental exposures that contribute to the similarity between co-twins ("shared" environment) having a small-tomoderate impact (0-30%) (55)(56)(57)(58)(59).One twin study examined the etiology of IPV victimization, estimating small-to-moderate genetic (15-25%) and very large nonshared environmental influences (75-85%) (60).Although twin studies of revictimization are scarce, one study found moderate genetic (rg = 0.22-0.37)and small nonshared environmental correlations (re = 0.05-0.16)on the association between maltreatment and subsequent sexual assault victimization (61)a form of violence often perpetrated by partners (62).The extent of the genetic and environmental sources of covariation between maltreatment and IPV remain, however, unexplored.
The presence of genetic influences on maltreatment and IPV may seem surprising.However, in a genetically informed design, when a heritable trait is associated with elevated risk for a particular exposure, the exposure itself will exhibit a heritable component.For example, since borderline personality is partly heritable and associated with maltreatment and IPV (63)(64)(65), genetic vulnerability to borderline personality may contribute to the genetic sources of covariation between these two experiences.Long recognized in criminological research (66), the role of personal characteristics in victimization remains understudied, possibly due to concerns that findings may be misrepresented as placing blame on victims (67,68).However, successful prevention requires support for victims, alongside measures targeting perpetrators, and comprehensive knowledge of the pathways leading to victimization, including personal vulnerabilities (46,69).This research can inform policy decisions about the prioritization of interventions aimed at reducing the risk of IPV among victims of maltreatment (8).For instance, if maltreatment is causally related to IPV, identifying specific pathways linking maltreatment to unsafe relationships, over and above their common risk factors (e.g., socioeconomic disadvantage, personality), may illuminate targets for secondary interventions aimed at preventing IPV in this group.Studying risk pathways in young adults seems crucial because early intimate partner relationships may underpin future family dynamics, making this research vital for informing interventions to disrupt the intergenerational transmission of violence (67,70).
In this study, we used a genetically informed design to address two research questions.
First, to what extent is the association between maltreatment and later IPV victimization attributable to common etiological factors?Based on findings concerning other forms of PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE revictimization (61,71), we expected moderate-to-large additive genetic and small-to-moderate nonshared environmental influences on this association.Second, does maltreatment exert a causal effect on later IPV victimization, over and above their common etiology?Considering evidence of both causal and common pathways linking these experiences, we predicted a significant but modest causal effect of maltreatment on later IPV victimization.Additionally, based on preliminary evidence of sex differences in the etiology of maltreatment and adult sexual assault (55,61), we explored possible etiological sex differences in the association between maltreatment and later IPV victimization.

Participants
We analyzed data from the Twins Early Development Study (TEDS), a longitudinal data collection involving twins born in England and Wales between 1994-1996.TEDS was approved by the ethics committee at King's College London; participants provided informed consent to participate.Zygosity was determined using DNA marker testing or a parent-reported questionnaire on physical similarity (72).For more details on recruitment procedures and sample representativeness, see (73,74).
From the original sample with non-missing data on the variables of interest (N = 13306), we excluded 512 participants due to serious medical and perinatal conditions or missing essential background variables (e.g., zygosity).The final sample comprised 12794 participants (6397 twin pairs), including 2224 MZ twin pairs (2792 women, 1656 men) and 4173 DZ twin pairs, of whom 2048 were same-sex (2496 women, 1600 men) and 2125 were opposite-sex.Participants were predominantly White (93.40%),heterosexual (79.14-84.75%),and in a relationship (58.16-TEDS participants reported changing gender at age 26 (0.95% of women-at-birth, 0.54% of menat-birth).Demographic information is reported in Table 1.

Measures
We analyzed retrospective self-reported continuous measures of maltreatment and IPV collected at ages 21 and 26.See Table 2 for details on items, scoring, and composite scores computation.Maltreatment was measured using the 'Life at 22+' scale at age 21 (75) and the 5item form of the Childhood Trauma Screener (CTS) (76) at 26. IPV from current or past partners was measured at age 21 using 6 items from the Centers for Disease Control and Prevention Violence Prevention questionnaire (77) and 4 items from the Adult Trauma Screener at 26 (78,79).Measures were selected by the TEDS team to capture the constructs of interest and for consistency with other large-scale surveys (e.g., UK Biobank).These measures of maltreatment (75,80) and IPV (78,81) have shown acceptable psychometric properties in previous studies and the current sample (see SM1).The use of different measures at different time points served as a conceptual replication to validate the generalizability of our findings.
For the descriptive analyses, we classified participants as victims if they scored 1.5 standard deviations (SDs) above the sample mean (M) on the composite scores of maltreatment and IPV, at each time point.This cut-off classified participants as victims if they had experienced maltreatment or IPV at least "sometimes" on average (or, for IPV at age 21, those who at least "agreed" to have experienced IPV).

Statistical analyses
Data preparation included assessing the psychometric properties of our measures, performing multiple imputation, and normalizing variables (SM1).The resulting dataset was used for all except descriptive analyses.We adopted a conservative significance level of p < .001 and considered estimates ≦.10 as very small, .11-.20 as small, .21-.30 as moderate, .31-.40 as large, ≧.40 as very large (82).We compared nested models using the likelihood ratio test (83).
We conducted descriptive analyses by inspecting how many participants exceeded our cutoffs for maltreatment and IPV.Next, we compared the proportion of participants reporting IPV among those classified as victims and non-victims of maltreatment.We examined phenotypic associations between maltreatment and IPV at each time point in a subsample comprising one randomly selected member from each twin pair (n = 6,397) to account for non-independence of observations.We estimated robust least squares regression models, given violation of linear regression assumptions (see SM2).We compared regression coefficients between sexes using two-sample z-tests (84).
Using bivariate correlated factors twin models (85), we estimated the proportion of variance in and covariance between maltreatment and IPV due to additive genetic influences (denoted as "A"), shared environmental influences ("C"), and nonshared environmental influences, encompassing measurement error ("E"), and the extent of the overlap in their etiological influences.Using bivariate sex limitation models (86,87), we explored possible sex differences in the etiology of the association between maltreatment and IPV (see SM3).Using direction-of-causation twin models (88,89), we tested the presence of a causal link from maltreatment to IPV (see SM4).Twin analyses were conducted in R using packages OpenMx (90) and umx (91).

Results
Prevalence rates are reported in Table 3.About 7% of participants reported experiencing maltreatment, about 8% reported IPV victimization.Slightly more women than men reported maltreatment; about twice as many women than men reported IPV.Participants who reported experiencing maltreatment were three times more likely than their peers to report IPV at age 21, and four times more likely at 26. Risk of IPV following maltreatment was comparable across sexes, but slightly higher in men.
Regression models revealed significant positive associations between maltreatment and Bivariate correlated factors twin models (Figure 2) indicated very large shared environmental, large nonshared environmental, and small-to-moderate genetic influences on maltreatment.Nonshared environmental influences accounted for a very large proportion of the variance in IPV, genetic influences were small-to-moderate, shared environmental influences were small at age 21 and nonsignificant at 26.The association between maltreatment and IPV was attributable to very large shared environmental, moderate-to-large genetic, and moderate nonshared environmental influences.We also found very large shared environmental and genetic correlations and small nonshared environmental correlations between maltreatment and IPV.
Sex limitation analyses (ST1) indicated quantitative sex differences in the environmental variance components at both time points.Specifically, equating shared and nonshared environmental components between women and men significantly worsened model fit (p < 0001), whereas equating the genetic component did not (p = 1.000).Inspecting estimates PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE 11 revealed minor sex differences in the etiology of maltreatment, including larger shared environmental influences in men at both time points and larger nonshared environmental influences in women at age 21.Qualitative sex limitation models failed to converge at both time points, precluding definitive conclusions on qualitative sex differences in our sample.
The direction-of-causation model stipulating a causal effect of maltreatment on IPV showed a comparable fit to the baseline noncausal model across time points and was therefore retained (model comparisons in ST2).The causal effect of maltreatment on IPV was significant and positive, small at age 21 and moderate at 26 (Figure 4).Alternative causal models testing a direction of causal effect of IPV on maltreatment could predictably be discarded, as IPV occurred after maltreatment.These models showed significant decrease in fit compared to the baseline; with the exception of the reciprocal model that showed comparable fit, but with the effect of IPV on maltreatment being negative and marginal at age 21 and nonsignificant at 26, suggesting a failure to accurately represent the data.

Discussion
Although individuals with a history of maltreatment are particularly vulnerable to IPV, research has made little progress in elucidating the mechanisms driving this form of revictimization.We addressed this gap using a quasi-experimental genetically informed design to discern causal and common pathways linking maltreatment to IPV victimization.Results indicated that environmental factors shared by co-twins, as well as genetic factors, mostly explain the association between maltreatment and subsequent IPV victimization.Furthermore, results supported the presence of a causal effect of maltreatment on later IPV victimization, which persisted even when adjusting for common etiological influences.

PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE 12
The common risk pathways to childhood maltreatment and intimate partner violence are mostly shared environmental and genetic in origin Shared environmental factors were particularly influential in explaining individual differences in exposure to both maltreatment and IPV victimization following maltreatment.Shared environmental influences on maltreatment have been previously documented (55).Since maltreatment is typically perpetrated by parents, it seems intuitive that its origins may lie primarily in environmental factors shared by co-twins raised together.However, negative parental behavior often varies between siblings, also as a result of genetically-influenced child traits (92,93).Therefore, our finding that maltreatment affected participants similarly regardless of their genetic similarity implies that abusive or neglectful parent behavior is shaped more strongly by the parent's characteristics than by their particular relationship with each child, in line with prior research (94).Shared environmental influences on the association between maltreatment and IPV victimization align with criminological findings on lifestyle and routine activities increasing revictimization risk (66,95).Activities like occupational demands in high-risk environments and housing instability are intergenerationally correlated.They can limit access to protective resources, potentially discouraging maltreatment survivors from reporting subsequent victimization and making them vulnerable targets for perpetrators (96-98) While the impact of such structural risk factors at a group level is known, our results highlight their potential role in driving individual differences too.Additionally, shared environmental correlations increased from age 21 to 26, which may reflect a longitudinal increase in the impact of shared influences, such as cultural norms, that persist when co-twins grow up (99,100).These mechanisms may contribute to the observed escalation in IPV risk among survivors of maltreatment from age 21 to PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE 13 26, although we cannot rule out that measurement discrepancies between these time points may also partly account for this finding.Over time, survivors of maltreatment may experience difficulties that gradually restrict the range of available behavioral responses and lead to 'thinner' social networks, increasing vulnerability to unsafe relationships (11,36,37).Conversely, the modest nonshared environmental influences on the association between maltreatment and IPV victimization imply that unique exposures -including distinct intimate partners -are less central to this revictimization pattern.These findings thus complement existing IPV theories focusing predominantly on perpetrator characteristics, by underscoring the importance of the victim's background in the pathways to IPV risk (46).
The second main source of covariation between maltreatment and IPV victimization was genetics.Since genes cannot affect victimization directly, genetic estimates likely reflect genetic propensities that increase susceptibility to experiencing or reporting victimization.For instance, perpetrators may seek partners displaying traits like high emotionality and agreeableness, which they view as exploitable (101,102).Other traits that have been associated with revictimization (e.g., low self-control (39,103), high risk-taking (104,105)), may also play a role in the association between maltreatment and IPV, contributing to its genetic component.Additionally, the genetic component of revictimization may encompass genetic influences on psychological processes, including cognitive biases, affecting how individuals perceive, interpret, and recall childhood experiences (106)(107)(108).Future research should clarify how heritable traits and psychological processes influence the selection and attraction of intimate partners among maltreatment survivors.Since genetic risk operates probabilistically and in combination with the environment, it can be mitigated by preventative measures.Alongside examining measures that account for individual-level vulnerabilities, future research should differentiate between pre-PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE 14 existing genetic effects, potentially exacerbating the impact of maltreatment (e.g., genetic risk for low self-control reducing resilience to trauma), from novel genetic effects exacerbated by maltreatment.

The causal effect of childhood maltreatment on intimate partner violence persists beyond their common risk pathways
Even when accounting for all possible common risk factors, maltreatment showed a smallto-moderate causal effect on later IPV victimization.Our findings thus offer robust evidence of the causal effect of maltreatment in exacerbating processes that may lead survivors into unsafe intimate relationships.Phenotypic studies have typically estimated a moderate-to-large effect when accounting for measured covariates.For instance, a cross-sectional study using structural equation modelling estimated a large effect of self-reported maltreatment on IPV victimization when adjusting for socioeconomic indicators known to confer risk for both experiences ( = .33)(48).A prospective study using multivariable logistic regression estimated a moderate effect of substantiated maltreatment on IPV when adjusting for individual-level risk factors (e.g., aggressive behavior) and family-level risk factors (e.g., social deprivation) (adjusted/unadjusted odds ratio = 2.12/3.19;(49).Our results demonstrate that the large effects identified using phenotypic methods, including our own regression analyses, may be inflated due to unmeasured sources of confounding.Genetically informed studies can thus guide future research into how risk for revictimization operates.
Although the precise causal pathways from maltreatment to IPV victimization have yet to be determined, various mediators have been identified, showing small indirect effect sizes.

PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE 15
cognitive processes including sense of agency and ability to discern trustworthiness (36,111,112), that are known to influence relationship dynamics (37,113,114).Future studies should examine how psychological processes impacted by maltreatment elevate risk of harmful intimate relationships.They should also assess the effect of interventions like trauma-focused cognitive-behavioral therapy on interpersonal outcomes, including the development of safe intimate relationships following maltreatment (115,116).Progress in this research is indispensable for enhancing prevention efforts and interrupting cycles of revictimization.

Strengths and limitations
This study is the first to apply a quasi-experimental genetically informed approach to study what drives the association between maltreatment and subsequent IPV victimization.By accounting for unmeasured sources of confounding, this approach strengthened our ability to draw causal inferences (52,117), providing robust evidence of both causal and common risk pathways from maltreatment to subsequent IPV victimization.This study also benefits from the largest sample size on this research question to date (N = 12794), increasing statistical power and confidence in the results.The compelling findings open avenues for further research aimed at illuminating intervention targets to prevent revictimization.Some limitations also warrant consideration.First, limited item availability precluded examining associations between specific types of maltreatment and IPV.However, polyvictimization is regrettably the norm -i.e., different forms of victimization frequently co-occur (118,119) -and different types of maltreatment all increase risk of IPV victimization (12).
Second, we used retrospective self-reports of victimization.While such measures may yield inflated prevalence, the converse is true when relying on prospective, official records of victimization (120).Moreover, self-report measures capture subjective perceptions of PATHWAYS FROM MALTREATMENT TO INTIMATE PARTNER VIOLENCE 16 victimization that are most strongly associated with mental health outcomes (121,122) and, possibly, vulnerability to IPV.Third, our sample lacked diversity, primarily comprising White heterosexual participants.Future research could investigate potential differences in etiological pathways to revictimization among marginalized groups, including ethnic minorities and LGBTQ+ individuals (123,124).Lastly, since some assumptions of the direction-of-causation model may be violated, such as no mutual effects between co-twins, (125), replication with alternative statistical approaches for causal inferences is warranted.
In conclusion, this study sheds light on the nature of the longitudinal association between maltreatment and IPV victimization.Our findings corroborate previous evidence that individuals exposed to maltreatment face a considerably increased risk of IPV, and further highlight an escalation in this risk over time.Genetically informed analyses revealed the substantial contribution of shared environmental and genetic factors common to maltreatment and IPV in driving their association.However, maltreatment remained causally related to IPV victimization even when accounting for their common etiology, albeit with a modest effect size.These findings not only offer novel theoretical insights into the processes underlying revictimization but also hold implications for policy and intervention strategies.In particular, they underscore the need for early interventions to mitigate the impact of maltreatment on intimate relationships, and the importance of tailored approaches to identification and management of IPV risk among maltreatment survivors, including measures tailored to personal and familial vulnerabilities.

Figure 4 .
Figure 4. Direction-of-causation model illustrating the causal impact of childhood maltreatment (CM) on intimate partner violence (IPV) at age 21 (4A) and 26 (4B).Nonsignificant paths and confidence intervals are omitted for ease of visualization.Direction of causation models replace one or more of the variance components for the common factors with regression paths directly from one phenotype to the other; therefore, factor components are not displayed.

Tables 364 Table 1 .
Demographic information 365 age 21, gap year or travelling and, at age 26, unpaid work.Relationship status: "In relationship" includes participants in exclusive and non-exclusive relationships not living with their partner at age 21, and "other" at age 26.Sexual orientation: "Bisexual" includes, at age 21, participants who reported being equally attracted to males and females or being attracted to the opposite sex sometimes; at age 26, it includes those who reported being pansexual or fluid; "Other" includes, at age 21, participants who reported little/no sexual orientation, being unsure, or not knowing, and, at age 26, those who reported being asexual or "other".